This study aimed to determine the value of HA/HAase for detecting bladder cancer on the basis of preceding statistical performance. PubMed, Springer Link, Web of Science and Cochrane Library were systematically searched to identify potentially relevant published articles by using the key words: "bladder cancer or bladder tumor or bladder carcinoma", "hyaluronic acid or hyaluronan", "hyaluronidase or HAase". The methodological quality of each study was assessed by QUADAS-2. According to the inclusive and exclusive criteria, 8 articles were identified and methodologically analyzed by STATA 12.0 software package.The results showed that the pooled sensitivity of HA and HAase was 0.832 (95% confidence interval [CI]: 0.798, 0.861) and 0.834 (95% CI: 0.756, 0.891) respectively, the pooled specificity was 0.886 (95% CI: 0.852, 0.913) and 0.860 (95% CI: 0.801, 0.904), and the area under the summary ROC cure (AUC) was 0.90 (95% CI: 0.87, 0.92) and 0.91 (95% CI: 0.88, 0.93), respectively. Simultaneously the diagnostic accuracy of the combination of HA and HAase showed that the pooled sensitivity was 0.908 (95% CI: 0.879, 0.931), the pooled specificity was 0.825 (95% CI: 0.789, 0.856) and AUC was 0.94 (95% CI: 0.91, 0.95), indicating a relatively higher accuracy than HA and HAase alone. This meta-analysis strongly suggests that HA/HAase could be used as biomarkers for the diagnosis of bladder cancer.

BackgroundClear cell renal cell carcinoma (CCRCC) is a prevalent urological carcinoma with high metastatic risk.Circular RNAs (circRNAs) have been identified as effective diagnostic and therapeutic biomarkers for CCRCC. This research aims to disclose the involvement of circRNA ribosomal protein L23a (circ_RPL23A) in CCRCC, and how it regulates carcinogenesis. MethodsWe performed quantitative real-time polymerase chain reaction (qRT-PCR) to examine circ_RPL23A, microRNA-1233 (miR-1233) and acetyl-coenzyme A acetyltransferase 2 (ACAT2). Cellular behavior detection included cell cycle, proliferation, apoptosis and metastasis, which were severally analyzed using propidium iodide (PI)-flow cytometry, 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT), Annexin V/PI-flow cytometry and transwell migration/invasion assays. ACAT2 and related proteins of cell cycle, epithelial-mesenchymal transition (EMT) were measured via western blot. Target relationship was analyzed via dual-luciferase reporter assay. A xenograft model was used to study circ_RPL23A action in mice. ResultsBoth in CCRCC tissues and cells, circ_RPL23A had a down-regulated tendency. Explicitly, circ_RPL23A overexpression inhibited cell cycle, proliferation and metastasis but enhanced apoptosis of CCRCC cells, whereas these effects of circ_RPL23A were dependent on the suppression of its target miR-1233. Besides, miR-1233 could target ACAT2 and circ_RPL23A regulated ACAT2 by sponging miR-1233. Also importantly, miR-1233 was a pro-cancer gene in CCRCC via targeting ACAT2. CCRCC tumor growth was also decreased in vivo by circ_RPL23A through miR-1233/ACAT2 axis. ConclusionAltogether, the circ_RPL23A/miR-1233/ACAT2 axis in this report provides an in-depth cognition for CCRCC pathogenesis and circ_RPL23A may has pivotal value in diagnosing and treating CCRCC.

Background Emerging evidence has noted the important participation of microRNAs (miRNAs) in several human diseases including cancer. This research was launched to probe the function of miR-381 in bladder cancer (BCa) progression. Methods Twenty-eight patients with primary BCa were included in this study. Cancer tissues and the adjacent normal tissues were obtained. Aberrantly expressed miRNAs in BCa tissues were analyzed using miRNA microarrays. miR-381 expression in the bladder and paired tumor tissues, and in BCa and normal cell lines was determined. The target relationship between miR-381 and BMI1 was predicted online and validated through a luciferase assay. Gain-of-functions of miR-381 and BMI1 were performed to identify their functions on BCa cell behaviors as well as tumor growth in vivo. The involvement of the Rho/ROCK signaling was identified. Results miR-381 was poor regulated in BCa tissues and cells (all p < 0.05). A higher miR-381 level indicated a better prognosis of patients with BCa. Artificial up-regulation of miR-381 inhibited proliferation, invasion, migration, resistance to apoptosis, and tumor formation ability of BCa T24 and RT4 cells (all p < 0.05). miR-381 was found to directly bind to BMI1 and was negatively correlated with BMI1 expression. Overexpression of BMI1 partially blocked the tumor suppressing roles of miR-381 in cell malignancy and tumor growth (all p < 0.05). In addition, miR-381 led to decreased RhoA phosphorylation and ROCK2 activation, which were also reversed by BMI1 (all p < 0.05). Artificial inhibition of the Rho/ROCK signaling blocked the functions of BMI1 in cell growth and metastasis (all p < 0.05). Conclusion The study evidenced that miR-381 may act as a beneficiary biomarker in BCa patients. Up-regulation of miR-381 suppresses BCa development both in vivo and in vitro through BMI1 down-regulation and the Rho/ROCK inactivation.

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